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Titolo:
Mutational spectrum of N-hydroxy-N-acetyl-4-aminobiphenyl at exon 3 of theHPRT gene
Autore:
Zayas-Rivera, B; Zhang, LF; Grant, SG; Keohavong, P; Day, BW;
Indirizzi:
Univ Pittsburgh, Dept Environm & Occupat Hlth, Pittsburgh, PA 15238 USA Univ Pittsburgh Pittsburgh PA USA 15238 at Hlth, Pittsburgh, PA 15238 USA Univ Pittsburgh, Magee Womens Res Inst, Dept Obstet Gynecol & Reprod Sci, Pittsburgh, PA 15238 USA Univ Pittsburgh Pittsburgh PA USA 15238 rod Sci, Pittsburgh, PA 15238 USA Univ Pittsburgh, Inst Canc, Pittsburgh, PA 15238 USA Univ Pittsburgh Pittsburgh PA USA 15238 st Canc, Pittsburgh, PA 15238 USA Univ Pittsburgh, Dept Pharmaceut Sci, Pittsburgh, PA 15238 USA Univ Pittsburgh Pittsburgh PA USA 15238 eut Sci, Pittsburgh, PA 15238 USA
Titolo Testata:
BIOMARKERS
fascicolo: 4, volume: 6, anno: 2001,
pagine: 262 - 273
SICI:
1354-750X(200107/08)6:4<262:MSONAE>2.0.ZU;2-Z
Fonte:
ISI
Lingua:
ENG
Soggetto:
HYPOXANTHINE-GUANINE PHOSPHORIBOSYLTRANSFERASE; POINT MUTATIONS; HUMAN-CELLS; CANCER; RNA;
Keywords:
HPRT; aminobiphenyl; denaturant gradient gel electrophoresis; TK6; mutational spectrum;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
16
Recensione:
Indirizzi per estratti:
Indirizzo: Day, BW Univ Pittsburgh, Dept Environm & Occupat Hlth, 260 Kappa Dr, Pittsburgh, PA 15238 USA Univ Pittsburgh 260 Kappa Dr Pittsburgh PA USA 15238 PA 15238 USA
Citazione:
B. Zayas-Rivera et al., "Mutational spectrum of N-hydroxy-N-acetyl-4-aminobiphenyl at exon 3 of theHPRT gene", BIOMARKERS, 6(4), 2001, pp. 262-273

Abstract

4-Aminobiphenyl is a human bladder carcinogen present in many environmental sources, including cigarette smoke. It can be metabolized in two steps tothe mutagen N-hydroxy-N-acetyl-4-aminobiphenyl (N-OH-AABP). In this study the mutational spectrum of N-OH-AABP-exposed human lymphoblastoid cells (TK6) was determined using HPRT as the target gene. Three large, HAT (hypoxanthine-aminopterin-thymidine)-cleaned TK6 cultures were independently treatedwith 20 muM N-OH-AABP for 24 h, allowed to recover for 4 days, then continuously exposed to 40 muM 6-thioguanine to select for induced mutants. Contemporary control cultures received vehicle in place of N-OH-AABP. N-OH-AABP treatment gave an 11-fold increase in mutation frequency. Mutations were delineated in exon 3 of the HPRT gene directly from genomic DNA extracted from both treated and untreated cells using the polymerase chain reaction, denaturing gradient gel electrophoresis (DGGE) and dideoxy sequencing. DGGE analysis showed N-OH-AABP increased both the number and type of mutations as compared with controls. The major background mutation was a G(197) --> A transition. The major N-OH-AABP-induced changes were G(209-211) --> T transversions (30 %), a seven-base repeat at position 185 (17 %) and an A(215) -->T transversion (2 %). The shift in the control spectrum of a transition tothat of transversions and insertions suggest that the electrophile N-OH-AABP forms bulky adducts at the same sites on exon 3 of HPRT as do many otherbulky electrophiles, causes replication errors by similar mechanisms, but induces at least one potentially signature mutation.

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Documento generato il 22/01/20 alle ore 06:49:48